Abstracts

RATIONALE:_Network oscillations occur in several areas of the limbic system, and may contribute to synaptic plasticity and epileptiform synchronization. Cholinergic agonists induce oscillations resulting from single neuron membrane properties implemented within the network by excitatory and inhibitory interactions. Here, we used slices of the rat subiculum to establish how network and single neuron membrane mechanisms participate to the rhythmic oscillations elicited by the cholinergic agent carbachol (CCh, 50-100 M). METHODS: Brain slices containing the subiculum were obtained from Sprague-Dawley rats and were maintained in vitro as previously described (Kawasaki et al., J Neurophysiol 82:2590-2601, 1989). Field potential and intracellular recordings were made according to standard procedures. RESULTS: Network oscillations (frequency=7-15Hz) were induced by CCh. They were abolished by an antagonist of non-N-methyl-D-aspartate (NMDA) receptors, but persisted with blockade of GABA receptor-mediated transmission. In addition, during application of glutamate and GABA receptor antagonists, single subicular cells generate burst oscillations at 2.5-5Hz when depolarized with steady current injection. These intrinsic burst oscillations disappeared during Ca2+ channel blocker application, intracellular Ca2+ chelation, or replacecement of extracellular Na+, but persisted when voltage-gated Na+ channels were blocked. These procedures caused similar effects on CCh-induced depolarizing plateau potentials that are contributed by a Ca2+-activated non-selective cationic conductance (ICAN). Network and intrinsic oscillations were abolished by atropine. CONCLUSIONS: Low frequency oscillations induced by CCh in the rat subiculum rely on a muscarinic receptor-dependent activation of an ICAN and are integrated within the network via non-NMDA receptor-mediated transmission. These oscillations may contribute to long-lasting changes in synaptic efficacy as well as to epileptiform synchronization.